Multi-user interference mitigation under limited feedback requirements for WCDMA systems with base station cooperation

One of the techniques that has been recently identified for dealing with multi-user interference (MUI) in future communications systems is base station (BS) cooperation or joint processing. However, perfect MUI cancellation with this technique demands severe synchronization requirements, perfect and global channel state information (CSI), and an increased backhaul and signaling overhead. In this paper, we consider a more realistic layout with the aim of mitigating the MUI, where only local CSI is available at the BSs. Due to synchronization inaccuracies and errors in the channel estimation, the system becomes partially asynchronous. In the downlink of wideband code division multiple access based systems, this asynchronism stands for the loss of the orthogonality of the spreading codes allocated to users and thus, for an increase in the MUI level of the system. In this contribution, we propose a framework for mitigating the MUI which builds in three main steps: definition of a cooperation area based on the channel characteristics, statistical modeling of the average MUI power experienced by each user and a specific spreading code allocation scheme for users served with joint processing. This code allocation assigns spreading codes to users in such a way that minimum average cross-correlation between active users can be achieved. Interestingly, these steps can be performed with a limited amount of extra feedback from the user's side

Expression of interleukin-8 receptors in endometriosis

PubMed ID: 15618253Background: Although the etiology of endometriosis is not well understood, chemokines and their receptors are believed to play a role in its pathogenesis. Therefore, we aimed to investigate the expression and localization of interleukin-8 (IL-8) receptors CXCR1 and CXCR2 in eutopic and ectopic endometrial tissues of women with endometriosis, and in endometrium of women without endometriosis. Methods: Ectopic (n = 27) and homologous eutopic endometrium (n = 25) from women with endometriosis and endometrium from women without endometriosis (n = 27) were used for immunohistochemical analysis of CXCR1 and CXCR2. Results: In normal endometrium, epithelial CXCR1 and CXCR2 immunostaining intensities were similar in the proliferative and secretory phase. Stromal CXCR1 expression was less then epithelial expression and did not show cyclical difference. No stromal CXCR2 expression was observed. In eutopic endometrium of women with endometriosis compared to endometrium of women without endometriosis, there was a significant increase in both proliferative and secretory phases for epithelial CXCR2 expression, and in proliferative phase for CXCR1 expression (P < 0.05). Both receptor immunoreactivities were significantly increased in the epithelial cells of ectopic endometrial tissues compared to that of normal endometrium (P < 0.05). Conclusions: These findings suggest that IL-8 and its receptors may be involved in the pathogenesis of endometriosis. © The Author 2004. Published by Oxford University Press on behalf of the European Society of Human Reproduction and Embryology. All rights reserved

Expression of interleukin-8 and monocyte chemotactic protein-1 in adenomyosis

WOS: 000232427600044PubMed ID: 15979992BACKGROUND: To clarify the inflammatory nature of adenomyosis, we aimed to investigate the expression of interleukin-8 (IL-8) and monocyte chemotactic protein-1 (MCP-1) by immunohistochemistry to determine their putative role in pathophysiology of adenomyosis. METHODS: Adenomyosis samples, with their eutopic endometrium, were collected from 30 women undergoing hysterectomy. Endometrium from 27 women without adenomyosis were also collected as a control group. Samples were grouped according to the menstrual cycle phase and examined by immunohistochemistry for IL-8 and MCP-1. RESULTS: In normal endometrium, secretory phase samples expressed higher levels of epithelial IL-8 than in proliferative phase samples (P = 0.01), and we observed a trend for an increased epithelial MCP-1 expression in the secretory phase samples compared with the proliferative phase samples (P = 0.07). Endometrial samples of women with adenomyosis did not show the same cyclic variation. In the secretory phase, eutopic endometrium of women with adenomyosis expressed lower levels of epithelial IL-8 and MCP-1 compared with normal endometrium (P < 0.05). The expression of epithelial IL-8 and MCP-1 was higher in the adenomyosis foci than the eutopic endometrium (P < 0.05). CONCLUSIONS: These findings may indicate that an intrinsic abnormality of inflammatory response may be present in eutopic endometrium of women with adenomyosis, and IL-8 and MCP-1 may contribute to the pathophysiology of adenomyosis